波形蛋白2通过其VCA区域激活血清反应元件，并在Rac的下游发挥作用。

Wave2 activates serum response element via its VCA region and functions downstream of Rac.

作者信息

Ishiguro Kazuhiro, Cao Zhifang, Ilasca Marco Lopez, Ando Takafumi, Xavier Ramnik

机构信息

Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.

出版信息

Exp Cell Res. 2004 Dec 10;301(2):331-7. doi: 10.1016/j.yexcr.2004.09.003.

DOI:10.1016/j.yexcr.2004.09.003

PMID:15530867

Abstract

WAVE2 is a member of the WASP/WAVE family of protein effectors of actin reorganization and cell movement. In this report, we demonstrate that WAVE2 overexpression induces serum response element (SRE) activation through serum response factor. A WAVE2 mutant lacking the VCA region did not induce SRE activation and actin polymerization. WAVE2-induced SRE activation was blocked by exposure of cells to Latrunculin A, or overexpression of actin mutant R62D. The DeltaVCA mutant inhibited Rac V12-induced SRE activation, suggesting that WAVE2 lies downstream of Rac. Similar deletion of the VCA domain of WASP attenuated Cdc42 V12-mediated SRE activation, suggesting that WAVE2 acts in relation to Rac as WASP acts in relation to Cdc42. WAVE2 overexpression did not activate NF-kappaB.

摘要

WAVE2是肌动蛋白重组和细胞运动的WASP/WAVE家族蛋白质效应器的成员。在本报告中，我们证明WAVE2过表达通过血清反应因子诱导血清反应元件（SRE）激活。缺乏VCA区域的WAVE2突变体不会诱导SRE激活和肌动蛋白聚合。将细胞暴露于Latrunculin A或过表达肌动蛋白突变体R62D可阻断WAVE2诱导的SRE激活。DeltaVCA突变体抑制Rac V12诱导的SRE激活，表明WAVE2位于Rac的下游。WASP的VCA结构域的类似缺失减弱了Cdc42 V12介导的SRE激活，表明WAVE2与Rac的关系如同WASP与Cdc42的关系。WAVE2过表达不会激活NF-κB。